Abnormally prolonged or asymmetric ventricular activation (conduction) is a frequent manifestation of cardiac disease and is characterized by QRS prolongation and/or axis deviation in the ECG. Although empirically presumed to result from delay in portions of the endocardial Purkinje network, there is some evidence to suggest that other mechanisms may also cause QRS prolongation in the electrocardiogram. Failure to appreciate the pathologic basis of the delay or asymmetry can (and does) result in inappropriate patient management and necessitates a more rational approach to ECG interpretation based on direct electrophysiologic observation and anatomic correlation rather than an empiric logic. The objectives of this study are to: (1) determine the various mechanisms resulting in delayed or asymmetric ventricular conduction and 2) to relate the abnormal electrophysiologic-anatomic findings to the surface potentials to achieve a more accurate prediction of the intracardiac mechanisms of QRS prolongation and axis deviation in man.